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Rheum Flashcards

1
Q

what is osteoporosis

A

loss of bone density without loss of bone mineralisation

results in increased susceptibility to bone fractures

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2
Q

what are the different types of osteoporosis

A

type 1 = post menopausal
type 2 = senile
secondary = disease process or medical tx

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3
Q

what are the risk factors for type 2 osteoporosis

A 
fhx
alcohol
RA
immobility
untreated menopause
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4
Q

what are the risk factors for secondary osteoporosis

A 
Steroid use 
Hyperthyroidism, hyperparathyroidism 
Alcohol
Thin BMI <18
Testeosterone 
Early menopause 
Renal failure 
Erosive bone disease 
Diet - low vit D or Ca
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5
Q

how do steroids cause osteoporosis

A

cortisol inhibits osteoblasts and activares osteoclasts

bone breaks down, reduced bone density

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6
Q

how does hyperthyroidism cause osteoporosis

A

thyroxine inhibits osteoblasts
increased bone breakdown than formation
also hypercalcaemia

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7
Q

what is the clinical presentation for osteoporosis

A

usually asymptomatic
fragility or pathological fracture

  • compression fracture - back pain, loss of height, loss of spine curve, hunched
  • colles fracture - distal radius
  • NOF fracture
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8
Q

3 cells within bone

A

osteoblasts - build bone secrete collagen and hydroxyapetite

osteoclasts - break down bone by secreting digestive enzymes and HCl breaks down bone -> releasing Ca and phosphate

osteocytes - osteoblasts stuck in bone matrix, act as mechanoreceptors

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9
Q

describe the effects of PTH

A

released from PTG in response to low serum Ca

1) leads to increased osteoclast activity - PTH stimulates RANK-l which stimulates osteoclasts to break down bone and release Ca
2) leads to increased Ca absorption - PTH acts on nephron, increases Ca reabsorption from DCT
3) increases synthesis of vit D - increases rate of vit D formation within kidney (higher vit D = increased Ca absorption from gut)

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10
Q

what does kidney disease lead to and why

A

renal osteodystrophy

kidneys produce less vit D

reduced Ca absorption from gut

leads to hypocalcaemia so PTH released

but PTH breaksdown bone -> weakening

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11
Q

why is there an increased risk of developing osteoporosis after menopause

A

menopause = low oestrogen

oestrogen inhibits osteoclasts - it stimulates OPG which inhibits RANK-l and thus prevents osteoclast activation

however, low oestrogen leads to less OPG and less inhibition of osteoclasts = greater bone breakdown = osteoporosis

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12
Q

which cells are activated more/less in osteoporosis

A

breakdown is faster than formation

so osteoclasts are activated more
osteoblasts are activated less

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13
Q

which bones are at greatest risk of fracture in osteoporosis

A

ribs
scapula
vertebrae

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14
Q

what is the FRAX tool

A

screening tool
assess person risk of fragility fracture over 10 years
performed in women 65+, men 75+
involves - age, BMI, comorbidities, smoking, alcohol, fhx, bone mineral density

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15
Q

what would blood tests shown in osteoporosis

A

all normal

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16
Q

what is the gold standard for osteoporosis investigation

A

DEXA scan
reading of the hip

generates 2 score - T and Z

T= value of bone density vs normal healthy population 
Z= value of bone density vs normal value for patient age
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17
Q

which score do we use to assess the severity of osteoporosis in DEXA

A

T-score

-1 = normal

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18
Q

management for osteoporosis

A

lifestyle advice - adequate ca and vit D intake

medical management
-bisphosphonates = aledronate or etidronate

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19
Q

how do bisphosphonates help osteoporosis

A

cause apoptosis of osteoclasts - stops bone degradation

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20
Q

side effects of bisphosphonaetes

A

oesophagtis
GORD
hypophosphataemia
osteonecrosis of jaw/external auditory canal

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21
Q

what is osteopenia

A

reduced bone density - not to the severity of osteoporosis

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22
Q

what is osteomalacia

A

disorder of impaired bone mineralisation and formation causing soft bones

loss of bone mineralisation but no loss of bone

23
Q

what is rickets disease

A

childhood presentation of osteomalacia

impaired mineralisation of cartilagenous growth plates

only happens if patient has osteomalacia during bone regrowth

24
Q

what is paget’s disease of the bone/osteitis deformans

A

increased bone turnover

associated with increased numbers of osteoclasts and osteoblasts

causes excessive bone breakdown and formation

leads to poor bone quality

25
Q

what are the risk factors for osteomalacia and rickets

A

those at risk of vit D deficiency

reduced sunlight
low intake of oral vit D
reduced intestinal absorption due to CF coeliac disease, gastrectomy
liver disease and CKD

26
Q

what is the cause of osteomalacia and rickets

A

lack of vit D so poor ca reabsorption from gut -> hypocalcaemia

27
Q

clinical presentation of osteomalacia

A

fatigue
bine pain
muscle cramps due to hypocal
pins and needles due to hypocal

proximal myopathy 
fractures 
waddling gait 
bone deformities 
trousseau sign (spasm in hand BP) 
chvostek sign (spasm of facial nerve)
28
Q

what is the clinical presentation of rickets

A

growth retardation
hypotonia
apathy
valgus and varus bone deformities

29
Q

how does vit D deficiency lead to osteomalacia and rickets

A

lack of vit D -> hypocalcaemia

bones will lack mineralisation as calcium is not able to form the bone mineral

leads to soft bones (osteomalacia) and inability to mineralise growth plates (rickets)

hypocalcaemia also leads to increased release of PTH - removes ca from bone making bones weaker

30
Q

what blood tests would you order for suspected osteomalacia/rickets

A
  • FBC to rule out infection or anaemia
  • U&Es for hypocalcaemia (due to lack of vit D), hypophosphataemia (excess PTH)
  • LFTs rasied ALP (from bone)
  • vit D (serum 25-hydroxy) low
  • PTH levels raised due to low Ca levels = secondary hyperparathyrodism
31
Q

how would osteomalacia appear on x-ray

A

transluscent
thin cortices
pseudo-fractures or looser zones = transevrse bands across bone

32
Q

how would rickets appear on x-ray

A

transluscent
thin cortices
wide epiphysis
clear bone deformities

33
Q

management for osteomalacia/rickets

A

ensure adequate vit D and calcium in body

vit D supplements - cholecalciferol to increase vit D and ca

34
Q

what is paget’s disease a disease of and how can it present

A

disease of osteoclasts - increased and disordered breakdown and turnover

rare <40

asymptomatic but can get pain in bones

  • pathological fracture = nerve compression
  • hearing loss due to narrow auditory foramen
35
Q

what blood test result would we get in pagets and what is the management

A

raised ALP

bisphosphonates

36
Q

what is the difference between seronegative and seropositive arthritis

A

seronegative = patient is not +ve for RF or anti-CCP

  • affects tendons and large joints
  • psoriatic arthritis ankylosing spondyloarthritis

seropositive = patients +ve for FR or anti-CCP
-have worse prognosis

37
Q

risk factors for rheumatoid arthritis

A

Female (3:1)

50-75 Years of Age

HLA-DR4 and HLA-DR1 Haplotypes

Family History

Smoking

Obesity

38
Q

risk factors for psoriatic arthritis

A

psoriasis

HLA-B27

39
Q

how would someone with rheumatoid arthritis present

A

symptoms

  • joint pain
  • joint swelling
  • fever
  • myalgia
  • fatigue

signs

  • rheumatoid nodules on elbows
  • anaemia - pallor
  • warm joints
  • joint deformities
  • uveitis
40
Q

hand deformities associated with RA

A

z-shaped deformitiy of thumb
swan neck
boutonnieres
ulnar deviation of MCP

41
Q

clinical presentation of psoriatic arthritis

A

symptoms

  • joint pain
  • joint stiffness
  • joint swelling
  • joint warmth

signs

  • skin changes
  • onycholysis
  • dactylitis
  • enthesitis
  • uveitis
42
Q

differentiating between RA and psoriatic arthritis

A

RA

  • affects MCPs, PIPs (NOT DIPs)
  • can affect shoulders, knees, ankles, elbows
  • morning stiffness
  • pain worse after REST, improves with ACTIVITY

PA

  • affects DIPs (NOT MCPs)
  • can affect spine, wrists, ankles, hands
  • pain worse after rest, improves with activity
43
Q

pathophysiology of rheumatoid arthritis

A

autoimmune attack of joints due to citrullination of proteins (arginine replaced with citrulline) which -> immune system unable to recognise cells

citrullination can occur due to smoking or genetic factors

autoimmune cells attack joint -> cytokine release (pro-inflamm = TNF-a, IL-1/6) -> systemic sx

attack of joint leads to proliferation of synovial joints -> panus (filled with granulation tissue)

overtime, the panus leads to damage of cartilage, soft tissue and bone

release of RANK-l -> increased osteoclast activation -> increased breakdown of joint

44
Q

what is the pathophysiology of psoriatic arthritis

A

T-cell mediated attack of joints

45
Q

blood test results for rheumatoid arthritis

A

FBC - anaemia of chronic disease

LFTs - raised CRP and ESR

RF - positive (indicated worse prognosis)

anti-CCP - positive, more specific for RA

46
Q

what are the investigations for psoriatic arthritis

A

psoriasis epidemiological screening tool - PEST

lack of RF and anti-CCP (bloods)

47
Q

x-ray results in hands and feet for rheumatoid arthritis

A

joint destruction and deformity
soft tissue swelling
periarticular osteopenia - redcued bone density
bony erosions

48
Q

x-ray results for psoriatic arthritis

A 
periostitis 
ankylosis - joining of bones 
osteolysis - bone destruction 
dactylitis - soft tissue swelling 
pencil in cup appearance - central erosions of bone
49
Q

special test for rheumatoid arthritis

A

DAS28 score - assess 28 joints

50
Q

management of RA

A

disease modifying anti-rheumatic drugs - methotrexate, leflunomide, hydroxychloroquine

if patient has DASS28 score of >5.1 qualify for biologic therapy - adalimumab, inflixamab (anti-TNF), rituximab (anti-CD20)

51
Q

how does methotrexate help in RA

A

inhibits action of dihydrofolate reductase (converts folic acid to tetrahydrofolate) - required for DNA synthesis

therefore limits anti-inflammatory effects by inhibiting IL-6/8, TNF-a

dampens down inflammation

52
Q

important measures while on methotrexate

A

prescribe folic acid
take FBCs and LFTs to ensure BM suppression and hepatotoxicity does not occur

take folic acid on different day to methotrexate

53
Q

management of psoriatic arthritis

A

similar to RA - NSAIDs, DMARDs, anti-TNF

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